Protective Effect and Mechanism of Total Flavones fromRhododendron simsiiPlanch Flower on Cultured Rat Cardiomyocytes with Anoxia and Reoxygenation

Author:

Jiao Yi1,Fan Yi-Fei1,Wang Yu-Ling1,Zhang Jun-Yan1,Chen Shuo2,Chen Zhi-Wu1

Affiliation:

1. Department of Pharmacology, Anhui Medical University, Hefei, Anhui 230032, China

2. Xinglin College, Liaoning University of Traditional Chinese Medicine, Shenyang, Liaoning 110167, China

Abstract

Many flavonoids have cardioprotection against myocardial ischemia/reperfusion (I/R) injury. Total flavones fromRhododendron simsiiPlanch flower (TFR) can protect myocardial ischemic injuries. However, its protective mechanism is still unknown. The present study was designed to investigate the mechanism of TFR on myocardial I/R and anoxia/reoxygenation (A/R) injuries. Rat model of myocardial I/R injury was made, and myocardial infarction was determined. A/R injury was induced in cultured rat cardiomyocytes; cellular damage was evaluated by measuring cell viability, LDH and cTnT releases, and MDA content. Expressions of ROCK1and ROCK2protein were examined by Western blot analysis, and K+currents were recorded by using whole-cell patch clamp technique. TFR 20~80 mg/kg markedly reduced I/R-induced myocardial infarction. TFR 3.7~300 mg/L significantly inhibited A/R-induced reduction of cell viability, LDH and cTnT releases, and MDA production. Exposure to A/R significantly increased ROCK1and ROCK2expressions in rat cardiomyocytes, but TFR 33.3~300 mg/L obviously inhibited this increase. 300 mg/L TFR significantly augmented inward rectifier K+current and other K+currents in rat cardiomyocytes. These results indicate that TFR has a protective effect on rat cardiomyocytes A/R damage, and the protective mechanism may be engaged with the inhibition of ROCK1and ROCK2and activation of K+channels.

Funder

National Natural Science Foundation of China

Publisher

Hindawi Limited

Subject

Complementary and alternative medicine

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